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Anaerobes (from chart) Flashcards

1
Q

General features of anaerobes

A
  • Mixed infections
  • remove toxic O2 forms
  • fermentation
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2
Q

Anaerobes live at _____

A

low redox potential (generated by other organisms)

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3
Q

Anaerobes produce ______

A

abcesses

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4
Q

Anaerobes (general) virulence factors?

A
  • Normal flora that enter unprotected areas
  • anaerobiosis either exits or generated by other organisms
  • tissue destructive enzymes -> abcesses
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5
Q

Common anaerobic abcesses…

A
  1. Abdominal
  2. Salpingitis
  3. Lung
  4. URT
  5. Brain
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6
Q

All anaerobic organisms

A
  1. Bacterioides fragillis
  2. Prevotella melaninogenica
  3. Porphyromonas gingivalis
  4. Fusobacterium
  5. Peptostreptococcus
  6. Propionibacterium
  7. Clostridium (bot, tet, perf, diff)
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7
Q

Anaerobic Gram Negative bacteria

A

Bacterioides, Prevotella, Porphyromonas, Fusobacterium

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8
Q

Anaerobic Gram Positive bacteria

A

Peptostreptococcus, Propionibacterium, Clostriduim

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9
Q

Anaerobe bacteria treatment

A

Drainage*

PenG

Metronidazole and Clindamycin

*Drainage allows O2 in

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10
Q

PenG not given to _____ and _____

Because they are ______________

A

Bacterioides and Prevotella

Beta-Lactam resistant

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11
Q

2nd line Antibiotics for Anaerobes

A

2nd and 3rd gen Cephalosporins and Carbapenems

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12
Q

Bacterioides Structure

A

Gram - Rod

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13
Q

Bacterioides features

A

60% of abdominal bacteria

Can live as monoculture

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14
Q

Bacterioides clinical

A
  • Colonic
  • 70% of anaerobic bacteremia

Most common

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15
Q

Bacterioides virulence

A
  1. Antiphagocytic capsule
  2. Enzyme production
  3. LPS
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16
Q

Bacterioides enzymes

A
  • SOD and Catalase
  • Neuraminidase and Heparinase
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17
Q

Prevotella Structure

A

Gram - Coccobacillus

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18
Q

Prevotella clinical

A
  • Oral
  • Brain and Lung abcesses
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19
Q

Prevotella enzymes

A

Collagenase

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20
Q

Porphyromonas structure

A

Gram - Rod

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21
Q

Porphyromonas Clinical

A
  • Oral
  • Gingivitis
  • Oral Abscess
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22
Q

Carriers of Porphyromonas

A

Warm and moist areas

-Axilla, groin, perineum

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23
Q

Fusobacterium structure

A

Gram - fusiform

24
Q

Fusibacterium locations

A

Oral and Colonic

25
Q

Fusibacterium Clinical

A

Infectious monoculture in osteomyelitis

26
Q

Peptostreptococcus structure

A

Gram + coccus

27
Q

Peptostreptococcus locations

A

Bacteremia

Pleura/lungs

28
Q

Propionibacterium acnes structure

A

Gram + pleiomorphic rod

29
Q

Propionibacterium location

A

-Skin (acne)

-Brain (abcess)

30
Q

Clostridium Structure

A

Gram + rounded ends

in pairs or short chains

31
Q

Clostridium bacteria are _______ and _________

A

Spore-formers

Strict anaerobes

32
Q

C. Botulinum clinical features

A

Flaccid paralysis (descending)*

-Dysphagia, Diplopia, Ptosis

*Starts with Cranial Nerves

33
Q

C. Botulinum Carriers

A
  • Home-_canned_ foods
  • Honey (floppy baby syndrome)
  • Wounds
34
Q

C. Botulinum Serotypes

35
Q

C. Botulinum virulence

A

AB Neurotoxin

  • B binds to Motor Neuron End plate
  • A prevents ACH vesicle fusion
36
Q

C. tetani incubation time

37
Q

C. tetani clinical

A

Rigid paralysis

  • trismus, ophisthotonos
  • death- from spasm interefering with respiration
38
Q

C. tetani carriers

A

Spores from penetrating fomites

Umbilical stump in neonatal tetanus

39
Q

C. tetani virulence

A

AB neurotoxin*

  • B binds to NMJ
  • A retrograde transported to presynaptic inhibitory neuron
  • Inhibit GABA release

*plasmid encoded tetanospasmin

40
Q

C. perfringens features

A

5 histotoxic strains

Others cause myonecrosis

41
Q

C. Sordelli causes…

A

Postpartum infection

42
Q

C. perfringens incubation

A

1-3 days infected wound suppurating

43
Q

C. perfringens clinical

A

Foul discharge, necrosis, toxemia, shock, death

44
Q

C. perfringens can also cause _____

A

Enteritis Necroticans (food poisioning)

**if ingested orally

45
Q

C. perfringens carriers

A

spores (in food poisioning)

Injury to tissues

Ischemia (anoxic environment)

*Polymicrobial if others use O2 to reduce oxygen presence

46
Q

C. perfringens virulence factors

A

a-toxin (phospholipase)

b-toxin (enteritis necroticans)

Hyaluronidase

Enterotoxin

47
Q

C. perfringens virulence effects

A

Leukocytosis

gas fermentation–> tissue distension–> vascular compression–> ischemia–> necrosis–> toxemia

48
Q

C. diff incubation

A

4-10 days secondary to Rx treatment

49
Q

Drugs that carry C. diff risk

A

Broad spec clindamycin

prolonged use of PPI

50
Q

C. diff clinical

A

May affect entirety or part of colon (= early watery diarrhea)

Pseudomembrane – leukocytes penetrate gut epithelium and form white-yellow exudate

51
Q

C. diff carriers/origin

A

Normal flora (impt for Treg development)

Antibiotics (disrupt flora)

DIsseminated in diarrhea

Nosocomial – 94%

52
Q

C. botulinum Tx

A

Trivalent (ABE) or Polyvalent Antitoxin immediately

NO AB because not infection

53
Q

C tetani vaccine

A

Tdap + boosters

54
Q

C. tetani Tx

A

-TIg antitoxin (early!)

–Tracheostomy

  • Muscle relaxant (MgSO4)
  • Metronidazole
55
Q

C. perfringens Tx

A

Amputation & Debridement

Penicillin, Metronizadole, Clindamycin

56
Q

C. diff Tx

A
  1. Stop Antibiotic, replinish flora
  2. fluids
  3. Anti-Toxin B Antibodies
  4. Vancomycin, Metronidazole
  5. Fidaxomicin
  6. Fecal replacement therapy

Bacteriology Lectures (14 decks)

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